Changes in cellular Ca2+ concentration affect multiple signaling processes in both excitable and non-excitable cells. Ca2+ signals can determine the nature and strength of neural connections in a circuit by specifying neurotransmitters and receptors. The extracellular medium, as well as intracellular stores, ...
Changes in cellular Ca2+ concentration affect multiple signaling processes in both excitable and non-excitable cells. Ca2+ signals can determine the nature and strength of neural connections in a circuit by specifying neurotransmitters and receptors. The extracellular medium, as well as intracellular stores, act as sources and sinks for signaling Ca2+. Most neuronal Ca2+ signals have been attributed to entry of extracellular Ca2+ through voltage-operated channels or ionotropic receptors. Intracellular Ca2+ channels such as the IP3 receptor and Ryanodine receptor are also present in both vertebrate and invertebrate neurons, but their function in determining synaptic specificity, connectivity and strength is less well understood. In Drosophila neurons, Ca2+ release through the IP3R also triggers Store-operated Ca2+ entry (SOCE) through the STIM/Orai pathway and together these mechanisms contribute to development and function of neurons that constitute the flight circuit. The papers in this research topic series will cover recent findings on IP3R and SOCE function in vertebrate and invertebrate neurons. The physiological and functional significance of IP3 mediated Ca2+ release and SOCE through STIM/Orai in mammalian neurons is an exciting new field of neuronal Ca2+ signaling, with important implications in cerebellar neurodegenerative disorders which will also be covered in this research topic series.
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